Fat is often given a bad rap. However, it has many vital purposes. These include (Inouye, 2005):
1. Phospholipid structure
2. Cell membrane structure
3. Storage of fat soluble vitamins
4. Production of hormones
5. Storage form of energy (adipose tissue)
6. Supply of energy through beta oxidation.
The goal with fat for a bodybuilder is to optimize the nutrient partitioning effect. Nutrient Partitioning can be defined as the distribution of ingested nutrients among basal metabolism, growth, tissue maintenance and repair, physical activity, and other forms of energy expenditure and nutrient storage. The goal is to partition nutrients away from fat storage, and towards these other vital functions that fats have, such as increased hormones.
Consuming the correct proportion of certain fats can help accomplish just this. Before proceeding, the various types of fats that exist must be opperationaly defined.
Saturated fats have a full quota of hydrogen’s and are therefore, very stable. Rich sources of these fats include butter, animal products, and coconut oil.
A diagram of a saturated fatty acid. The “OH” is the acid tale, or hydroxyl group.
Unsaturated fatty acids have double bonds and therefore, less hydrogen’s. Two classifications of unsaturated fats are: monounsaturated and polyunsaturated fats. Monounsaturated fats have one double bond, and are therefore, much more reactive (less stable). Rich sources of these fats include grape seed oil, olive oil, canola, peanut oil and avocado.
Figure two is a diagram of a monunsaturated fatty acid. Notice it contains only one double bond on the carbon atoms.
Polyunsaturated fats contain 2 or more double bonds. Rich sources of these fats include safflower, flax, fish, and walnuts.
Figure 3 depicts the polyunsaturated fatty acid, Alpha-linolenic Acid.
The length of a chain of carbons also determines the classification of the fatty acid.
>8 are short chain fatty acids
8-12 carbons are medium chain
16 + = long chain fatty acids
Evidence suggests that short and medium chain fatty acids can actually diffuse into mitochondria without carnitine transferase, which is important for their ability to be oxidized. This is why medium chain FFA's are often used for say malabsorbtion sydromes of fats.
There are three main differences between long and medium chain fats:
1. Chain length
2. Solubility - medium chains are more soluble in water
3. Medium chains can diffuse into the mitochondria without carnitine transferase
In this context, medium chains TG's are actually preferentially oxidized.
One of the ways to measure if a food is being used for energy or not is to measure oxygen consumption before and after the nutrient is taken in.
In one study (Brody, 2003) people consumed 45 grams of long or medium chain fatty acids. Oxygen was measured to determine energy used. 02 consumption increased slightly in the long chain condition, but a larger increase occurred in medium chain condition. This is consistent with long chain FFA's being first stored as fat, with medium chain ffas being oxidized instead. In 6 hours following test meals, 13 % of medium chain and 4 % of long chain were completely oxidized. Thus, fat oxidation is relative to the fat substrate.
Therefore, medium chain FFA's are less likely to be stored as fat, and more likely than long chain FFA's to be used as fuel. However, this depends on the type of long chain triglyceride. For instance, essential fats are long chained fatty acids; but, they have been found to increase insulin sensitivity, thermogenesis, anabolic hormones, anti-inflammatory cytokines, among numerous other benefits (Wilson, G. 2003).
For more information on essential fatty acids, refer to Wilson, G (2003) Essential Fatty Acids - An In Depth Analysis.
It has been shown that fat plays a key role in the formation of anabolic hormones.
Goldin et al. (1994) investigated the effect of dietary fiber and fat on serum sex hormones in premenopausal women. Participants consisted of 48 women, who’s diets were high in fat (40% of calories as fat) and low in fiber (12 g/day). Participants then changed to a low-fat (20-25% calories as fat) and high fiber (40 g/day) diet. Results found that there were significant decreases in serum concentrations of estrone, estrone sulfate, testosterone, androstenedione, and sex hormone binding globulin (SHBG) and near significant decreases in estradiol and free estradiol.
Hamalainen et al. (1994) had participants decrease fat from 40-25% and found a decrease in the serum concentrations of androstenedione, testosterone and free testosterone.
Ingram (1987) randomly assigned thirty-three women in good health to commence either a standard diet (deriving 40% of their energy from fat) or a low-fat diet (deriving 20% of their energy from fat), for two months, in a cross over study, which lasted a total of 16 weeks. Low-fat diets appeared to decrease levels of both non-protein-bound estradiol (1.48 down to 1.27%; P = .07) and non-protein-bound testosterone (1.06 down to 0.86%; P = .11). Cholesterol levels were lowered by the low-fat diet and were significantly associated with estradiol, testosterone, and dehydroepiandrosterone.
In a related study, Reed et al. (1987) found similar results. He also found that Changing the diet from one with a high fat to low fat content (less than 20 g fat/day) for a further two week period resulted in a significant reduction in mean plasma cholesterol levels (p less than 0.001); while the mean SHBG levels increased (p less than 0.01).
Volek et al. (1997) found that subjects eating a moderate fat diet exhibited higher testosterone levels than subjects eating low-fat diet. Additionally, they found that monounsaturated and saturated fat raise testosterone levels, but polyunsaturated fat do not.
As discussed, Reed et al. (1987) found that Changing the diet from one with a high fat to low fat content (less than 20 g fat/day) for a further two week period resulted in a significant reduction in mean plasma cholesterol level (p less than 0.001) while the mean SHBG level increased (p less than 0.01). Thus, another action of fat is to decrease levels of SHBG.
Concerning SHBG, this binds testosterone, temporarily constraining steroid hormones from exerting their activities. Therefore, by lowering levels of SHBG, you will raise the amount of free steroid hormones in the body.
While saturated fats clearly are beneficial for raising anabolic hormones, evidence suggests they have several deleterious effects. Here is a quote from Wilson, G. (2003) explaining one of these effects:
[ QUOTE ]
If you have read any of our articles, you know just how valuable insulin sensitivity is. Simply put, increased sensitivity promotes a much greater anabolic response to insulin and increases your fat-burning ability immensely, while insulin resistance leads to elevated fat storage, reduced hypertrophy, and increased susceptibility to diseases such as diabetes. For more, study the following articles: Metabolic Primer Part I, and Endocrine Insanity Part III.
Here is the exciting part: studies show omega-3s can increase insulin sensitivity drastically, while its counterpart--omega-6s--in higher dosages may lead to insulin resistance.
For instance, a fascinating study was performed on rats using high-fat diets and various lipids to assess their effect on bodyweight regulation, adiposity, and metabolism. Results showed that rats who consumed high amounts of saturated or n-6 polyunsaturated fatty acids became obese, insulin resistant, and gained the most fat, while fish oils showed to be a superior fat in the experiment .
Another study stated that the negative effects of a high-sucrose diet, which induced insulin resistance and mild glucose intolerance, were counteracted by enhanced dietary intake of omega-3 polyunsaturated fatty acids .
Storlien LH et al. tested the effects of certain fats on rats. Subjects who had diets rich in polyunsaturated (omega-6) fatty acids developed severe insulin resistance. Afterward, they substituted 11% of the fatty acids in the polyunsaturated fat diet with long-chain omega-3 fatty acids from fish oils. The omega-3s were shown to effectively normalize insulin action .
Furthermore, Chicco A et al. composed a diet with 7% of the calories coming from cod liver oil--which is rich in omega-3 fatty acids--on male Wistar rats. The end results showed a significant reduction in plasma insulin levels throughout the day, due to enhanced insulin sensitivity .
Popp-Snijders C et al. performed an excellent study for the effects of Omega-3s on diabetics. Six non-insulin-dependent diabetics supplemented with just 3 g of the omega-3 fatty acids daily, over an 8 week time span. The subjects showed enhanced insulin sensitivity and lower plasma triglyceride levels .
Another experiment was performed on rats. First, they implemented a diet high in omega-6 and saturated fatty acid, which again lead to insulin resistance. Afterward, they replaced simply 6 percent of the linoleic omega-6 fatty acids from safflower oil with long-chain polyunsaturated omega-3 fatty acids from fish oil. This resulted in the prevention of insulin resistance .
It should be noted that in Western society diabetes has become a prevalent disease. This can be largely attributed to the lopsided ratio of omega-6:3 fatty acids. Diabetics will want to take close notice of these results, and adjust their diets accordingly .
So, as you see, a diet rich in Omega-6s can lead to insulin resistance, while a diet full of Omega-3s will inevitably increase insulin sensitivity [39,40,14].
[/ QUOTE ]
In summary, a high dosage of omega 6 or saturated fatty acids increases insulin resistance and fat gain. While omega 3 fatty acids have been shown to enhance insulin sensitivity and fat oxidation.
A high fat diet has also been shown to decrease satiety. Here is another quote from Wilson, G. (2003) in his article on satiety explaining:
[ QUOTE ]
Studies show that humans adapt very quickly to high fat diets (HFD), which subsequently decreases the satiating response to nutrients. For instance, Cunningham et al. showed that consumption of a high-fat diet for two weeks led to an acceleration in the gastric emptying rate of high-fat test meals . However, CCK is still raised very high during HFD, making these results rather strange . To test the mechanisms by which this adaptation occurs, Covasa and Ritter injected CCK into rats on low fat diets and high fat diets . The former group had a much slower rate of gastric emptying (26.2-55.1%) than the later group (10.0-31.7%). This shows that HFD may cause subjects to be insensitive to CCK’s satiating effects.
To further investigate this, French et al. had 12 male subjects consume a high-fat diet (58% energy) for two weeks, testing levels of cholecystokinin (CCK), food intake, and subjective feelings of hunger and fullness . The results showed a significant enlargement in the average daily food consumption, increasing feelings of hunger and declining fullness. And again, CCK was substantially higher, further supporting the hypothesis that high-fat diets reduce the body’s sensitivity to this hormone.
Castiglione, Read, and French sought to test whether this effect on gastric emptying was nutrient-specific . Studies were carried out on eight healthy, free-living male volunteers between the ages of 19 and 26. Their original fat intake was between 30-40%. In the test they increased this to 55% for 14 days. They then gave them high-fat and high-carbohydrate meals. The high carbohydrate meals had nearly the same rate of gastric emptying before and after the experiment. However, the rate of lipid emptying was much faster, consistent with the previous experiments. This shows HFD adaptations are nutrient-specific to fats, and not to carbohydrates.
Now, most athletes never would have this much fat in their diet. However, this does show the folly in excessively high-fat/low-carb diets, which not surprisingly often advocate the wholly ignorant, logically invalid, and completely unscientific protocol of fat and fiber post-workout. Moreover, you can see that people who eat junk food constantly (i.e. pizza) are going to be much more susceptible to continued binges than someone on a lower fat diet. To exemplify the harm in this adaptation, rats fed the same amount of fat at a slow rate consumed less energy per day, had longer between-meal intervals, and gained less weight over a two-week period than after infusion of fat at a more rapid rate . So, those reading need to take a close look at their diet, and be sure they are not consuming excessive amounts of fat right now.
[/ QUOTE ]
Fat efficiency is therefore, of the utmost importance, as consuming to much fat is unhealthy, will promote fat storage, lower satiety, among numerous other negative effects.
While the polyunsaturated fats Alpha-Linolenic Acid and Linoleic Acid have been thoroughly investigated by Wilson, G. (2003) questions still remain on the consumption of various other fats, especially when considering that polyunsaturated fatty acids are ineffective in raising testosterone levels.
Bodybuilders are often proponents of large consumptions of meats such as steak which are rich in saturated fatty acids. As displayed, this would elicit anabolic benefits such as increased testosterone, but it also will have deleterious effects such as lowered insulin sensitivity.
However, while medium chain triglycerides are a type of saturated fat, studies have found that they are excellent for increasing fat oxidation, contrary to reports on supplementation with other saturated fatty acids. If these fats therefore elicited the same anabolic benefits as other saturated fatty acids, they would be of practical importance to the athlete.
In this context, the purpose of this thread is to discuss how to optimize fat efficiency in the diet. Of particularly interest is the effect of medium chain triglycerides on hormones such as testosterone. Posts on the benefits of any type of fat, scientific studies to support claims, and theoretical rationales behind these claims are promoted.